40 articles - From Friday May 20 2022 to Friday May 27 2022
Guidelines, position statements, white papers, technical reviews, consensus statements, etc…
meta-analyses and systematic reviews
RCT, clinical trials, retrospective studies, etc…
| Am J Kidney Dis |
Efficacy of Potassium Supplementation in Hypokalemic Patients Receiving Peritoneal Dialysis: A Randomized Controlled Trial. Compared to reactive potassium supplementation when serum potassium falls below 3.5 mEq/L, protocol-based oral potassium treatment to maintain serum potassium concentration in the range of 4-5 mEq/L may reduce the risk of peritonitis in patients receiving PD who have hypokalemia. |
Performance of the 2021 Race-Free CKD-EPI Creatinine- and Cystatin C-Based Estimated GFR Equations Among Kidney Transplant Recipients. Rationale & objective Race-free eGFR equations incorporating creatinine with and without cystatin C were recently developed and recommended for routine use. However, the performance of these equations among kidney transplant recipients remains unknown. Study design Cross-sectional study to validate the new race-free CKD-EPI equations (2021 CKD-EPI equations in the kidney transplant population. |
| Clin J Am Soc Nephrol |
Mechanical Circulatory Support: Primer for Consultant Specialists. Generally speaking, these tools are supportive therapy to allow for organ recovery but, at times, require transition to long-term mechanical support. This review will examine nonrenal extracorporeal life support for cardiac and pulmonary support as well as other mechanical circulatory support options. This is intended as a general primer and overview to assist nephrologist consultants participating in the care of these critically ill patients who often experience acute renal injury as a result of cardiopulmonary shock and from their exposure to mechanical circulatory support. |
Medicare Bundled Payment Policy on Anemia Care, Major Adverse Cardiovascular Events, and Mortality among Adults Undergoing Hemodialysis. The Medicare reimbursement policy and Food and Drug Administration-recommended erythropoietin-stimulating agent dosing changes were associated with lower erythropoietin-stimulating agent use and lower hemoglobin levels. These changes in anemia care were associated with lower risks of major adverse cardiovascular event, stroke, mortality, and heart failure but higher risk of acute myocardial infarction among adults receiving hemodialysis. |
| J Am Soc Nephrol |
Effects of Short-Term Potassium Chloride Supplementation in Patients with Chronic Kidney Disease. In patients with CKD stage G3b-4, increasing dietary potassium intake to recommended levels with potassium chloride supplementation raises plasma potassium by 0.4 mmol/L. This may result in hyperkalemia in older patients or those with higher baseline plasma potassium. Longer-term studies should address whether cardiorenal protection outweighs the risk of hyperkalemia. |
| Kidney Int |
Bruceine A protects against diabetic kidney disease via inhibiting galectin-1. Here, we identified Bruceine A as a kidney protective molecule against a model of diabetic kidney disease in db/db mice with potent anti-inflammatory activity both in vitro and in vivo. Mechanistically, by selectively binding to the conserved carbohydrate-recognition domain of galectin-1 and disrupting the interaction between galectin-1 and the receptor for activated protein C kinase 1, Bruceine A was found to inhibit galectin-1-mediated inflammatory signal transduction under high glucose stress in rat mesangial HBZY-1 cells. Thus, our findings reveal Bruceine A as an unidentified galectin-1 inhibitor affording significant protection against diabetic kidney disease and may provide novel pharmacological therapeutics for the disease. |
Protective mechanisms harnessing against injurious heme and preventing kidney damage in STEC-HUS: toward new therapies? When hemoglobin and heme released from ruptured erythrocytes interact with the kidney cells, this can result in platelet activation, vascular inflammation and occlusion, and kidney injury. Pirschel et al now report that in the absence of protective mechanisms against free hemoglobin and heme, heme-induced kidney injury can be exacerbated. Therapeutic strategies should therefore also target heme-mediated deleterious effects in (severely ill) patients with Shiga-toxin-producing enterohemorrhagic Escherichia coli hemolytic uremic syndrome. |
Renoprotection by GDF15 and Klotho: birds of a feather flock together. Growth differentiation factor 15 is a potential renoprotective factor whose expression is induced primarily at the proximal tubular site after kidney injury. Valiño-Rivas et al confirmed the protective effect of growth differentiation factor 15 against different types of kidney injury and further identified that growth differentiation factor 15 also induces kidney expression of another renoprotective factor, Klotho. Surprisingly, Klotho expression is apparently enhanced in the proximal tubule, suggesting the cooperative action of the 2 renoprotective factors at this injury-prone site. |
Rho-associated, coiled-coil-containing protein kinase 1 regulates development of diabetic kidney disease via modulation of fatty acid metabolism. We found that high-fat diet-induced obese ROCK1 knockout mice exhibited reduced albuminuria and histological abnormalities along with the recovery of impaired fatty acid utilization and mitochondrial fragmentation. Mechanistically, we found that ROCK1 regulates the induction of critical mediators in fatty acid metabolism, including peroxisome proliferator-activated receptor gamma coactivator 1a, carnitine palmitoyltransferase 1, and widespread program-associated cellular metabolism. Thus, our findings highlight ROCK1 as an important regulator of energy homeostasis in mesangial cells in the overall pathogenesis of diabetic kidney disease. |
Should we consider calcimimetics as a therapeutic option for nephrotic syndrome? Using a CaSR knockdown in podocytes and a podocyte-specific CaSR knockout in mice, Mühlig et al uncovered a stabilizing role for actin cytoskeleton and cell adhesion. Short-term alleviation of albuminuria and proteinuria was observed in 4 children treated with cinacalcet. Here we discuss the potential mechanisms whereby CaSR displays a favorable effect in podocytes and the context in which calcimimetics may alleviate nephrotic syndrome. |
| Nephrol Dial Transplant |
Evaluation of renal oxygenation by BOLD-MRI in high-risk patients with type 2 diabetes and matched controls. T2DM patients with normal to moderate CKD does not seem to have lower renal oxygenation when measured with BOLD-MRI and TLCO. BOLD-MRI has a low intra-individual CV and seems like a reliable method for investigation of renal oxygenation in T2DM. |
Metabolic dysfunction-associated fatty liver disease predicts new onset of chronic kidney disease better than does fatty liver or nonalcoholic fatty liver disease. MAFLD is modestly and independently associated with new onset of CKD and predicts the risk for development of CKD better than does FL or NAFLD. |
The risks associated with percutaneous native kidney biopsies: a prospective study. This is the first multicentre prospective study showing that percutaneous native kidney biopsies are associated with a 5% risk of a major post-biopsy complication. Predictors of increased risk include higher plasma creatinine levels, liver disease, and a higher number of needle passes. |
Uromodulin and its association with urinary metabolites: the German Chronic Kidney Disease Study. We identified urinary metabolites associated with urinary and serum uromodulin. sUMOD and the sMS were associated with lower risk of adverse kidney events among CKD patients. Higher levels of sUMOD and sMS may reflect a higher number of functional nephrons and therefore a reduced risk of adverse kidney outcomes. |
Plenty of the editorials are available as full text through the publisher website using the provided link
| Am J Kidney Dis |
Renal Denervation: A Review. In the search for interventions which lower blood pressure without reliance upon adhering to a regimen requiring daily ingestion of medication, or repeated physical activity, device-based methods that denervate the renal arteries have emerged as a potential complement to standard antihypertensive treatments. At least three different approaches to renal artery denervation are under active investigation, including the use of radiofrequency energy, or ultrasound, or the injection of neurolytics into the renal perivascular tissue. In this review we cover what is currently known about the mechanisms of antihypertensive effect of renal denervation, summarize the efficacy and safety of renal denervation using recent controlled trial publications in a number of hypertensive populations, and conclude with some thoughts about challenges in the field including optimizing patient selection for the procedure, and what the reader can expect in the near future in this rapidly developing field. |
| Clin J Am Soc Nephrol |
| Clin Kidney J |
Primary hyperoxaluria type 1 in developing countries: novel challenges in a new therapeutic era. In this review we discuss the current situation of PH1 in DC as well as the accessibility challenges and the advantages of using promising novel therapeutics to bridge the currently existing gap. We also provide an overview of an integrated approach to ensure equitable access of sustainable therapeutics to PH1 patients in DC. This is expected to reduce global PH1 healthcare disparities, improve its standard of care and reduce disability linked to extrarenal complications of PH1 by implementing personalized medicine. |
Primary hyperoxaluria type 1: novel therapies at a glance. Pharmacological compounds directly inhibiting GO or LDH are also under development and could be of special interest in developing countries where RNAi therapies may not be readily available in the near future. Approaches to manipulate the intestinal microbiome with a goal to increase oxalate degradation or to stimulate secretion of oxalate into the intestine from plasma are also under development. Overall, we appear to be entering a new phase of PH treatment, with an array of promising approaches emerging that will need optimization and evaluation to establish long-term efficacy and safety. |
Primary hyperoxaluria type 1: pathophysiology and genetics. It is caused by a deficiency in the liver-specific enzyme, alanine:glyoxylate aminotransferase (AGT), a pyridoxal-5'-phosphate (PLP)-dependent enzyme involved in the metabolism of glyoxylate. The excessive endogenous synthesis of oxalate that ensues leads to hyperoxaluria, and the crystallization of the poorly soluble calcium salt of oxalate is responsible for a severe kidney stone disease, which can progress to end-stage renal disease, systemic deposition of oxalate and death. Knowledge about metabolic precursors of glyoxylate and oxalate, molecular pathology of AGT and analytical methods for diagnosis and clinical assessment have allowed a better understanding of the mechanisms underlying PH1 and opened the door to new therapeutic strategies. |
Primary hyperoxaluria type 1: time for prime time? Primary hyperoxaluria type 1 (PH1) is an autosomal recessive disease due to a mutation in the includes contemporary reviews of the pathophysiology and genetics, (conventional) medical therapeutic management, urological therapeutic management and novel therapies (including not only RNAi, but also other therapeutic perspectives). The specific opinions of both adult and paediatric nephrologists will be compared and the ethical issues, as well as challenges faced by physicians and patients in developing countries, will also be discussed. Despite al the accomplishments, there are still looming questions that require further investigation and discovery. |
Primary hyperoxaluria type 1: urologic and therapeutic management. Percutaneous nephrostolithotomy might intuitively seem favorable given the shortest drain duration and the ability to treat larger stones efficiently but, similar to SWL, rapid chronic kidney disease (CKD) progression has been seen postoperatively. Ureteroscopy is therefore generally the safest option, but considerations regarding stent encrustation, the growth of residual fragments and the large volume of stone often faced may limit this approach. The surgeon must balance the above with consideration of the patient's CKD status when considering a plan of monitoring and treating stones in PH. |
Primary hyperoxaluria: the pediatric nephrologist's point of view. We review the various manifestations of pediatric hyperoxaluria, treatment options for children with preserved kidney function and appropriate dialysis regimens. Liver or combined liver/kidney transplantation is currently the only definitive treatment for primary hyperoxaluria type 1, but novel RNA interference treatments offer hope for the future. Finally, we address the medical and ethical dilemmas facing pediatricians treating children with hyperoxaluria. |
Treatment of primary hyperoxaluria type 1. Liver transplant can be isolated or combined with kidney transplantation in a sequential or simultaneous fashion. Isolated kidney transplantation is generally reserved for pyridoxine-sensitive patients only. Although liver transplantation is curative for PH1 and kidney transplantation treats ESKD, ensuing necessary immunosuppression and potential allograft dysfunction impart significant long-term risks. |
| Nat Rev Nephrol |
Letters to the editors and authors’ replies
| Kidney Int |
all remaining publications eg case reports, images of the month, etc…
| Am J Kidney Dis |
| Clin J Am Soc Nephrol |
| Kidney Int |
| Nephrol Dial Transplant |